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Brain dysfunctions: Shared mechanisms in fragile X syndrome, autism and schizophrenia
Date:9/22/2013

herited intellectual disability. Patients often show autistic-like behavior, anxiety, aggression, hyperactivity and self-injurious behavior. The condition is caused by the absence of the Fragile X Mental Retardation protein (FMRP) that is involved in supplying the correct building blocks for the synapse. Claudia Bagni's team had previously demonstrated that FMRP forms a complex with CYFIP1 to regulate this supply.

Shaping our synapses

Bagni's group has now identified a key function of CYFP1 at synapses. CYFIP1 orchestrates two biological processes: together with FMRP, it acts to regulate the protein supply at synapses and when bound to another complex (WRC), controls actin polymerization, a scaffold of brain cells. These findings lead to the "hub" model, in which the same complex, having CYFIP1 at the center, might be affected in apparently different diseases. A disrupted balance between the two functions results in abnormal contacts between brain cells. Silvia De Rubeis, Emanuela Pasciuto and Claudia Bagni (VIB/KU Leuven/Tor Vergata-Rome) have exposed the molecular mechanisms that ensure that this balance is maintained.

The important function of CYFP1 was underlined further by the discovery that many proteins that interact with CYFP1 were already associated with (hereditary forms of) brain conditions. The VIB scientists suggest that mutations in the proteins working together with CYFIP1 might perturb the balance of the interaction networks thereby triggering a spectrum of pathological processes at synapses that can lead to a broad range of clinical manifestations such as intellectual disabilities, autism and schizophrenia. This study offers new perspectives for a better understanding of these still not understood brain conditions.


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Contact: Sooike Stoops
info@vib.be
32-924-46611
VIB (the Flanders Institute for Biotechnology)
Source:Eurekalert

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